29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Data from deformation-based magnetic resonance imaging morphometry demonstrated a Parkinson's disease-specific brain network had more atrophy in the diffuse malignant subtype, with the mild motor-predominant subtype having the least atrophy. 4 key findings →
Design: longitudinal study Participants: 223 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The utility of plasma total tau level as a prognostic marker for cognitive decline and dementia is not well understood. 4 key findings →
Design: cohort study Participants: 458 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). 5 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials. 3 key findings →
Design: longitudinal study Participants: 233 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The purpose of this systematic review and meta-analysis was to evaluate the performance of cerebrospinal fluid (CSF) beta amyloid 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) as potential diagnostic biomarkers for idiopathic normal-pressure hydrocephalus (iNPH) and to assess their utility indistinguishing patients with iNPH from those with Alzheimer disease (AD) and healthy normal controls. 4 key findings →
Design: systematic review Participants: 413 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative processes encompass a large variety of diseases with different pathological patterns and clinical presentation such as Amyotrophic Lateral Sclerosis (ALS), Alzheimer Disease (AD) and Parkinson's disease (PD). 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The findings suggest that detection of αSyn oligomers by αSyn-PMCA in the CSF of patients affected by PD may offer a good opportunity for a sensitive and specific biochemical diagnosis of the disease. 5 key findings →
Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among the nonmotor symptoms in Parkinson's disease (PD), cognitive impairment is one of the most common and devastating. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The best discriminators between probable/definite bvFTD and PSY were the levels of CSF NfL (area under the curve [AUC] 0.93, P < .001, 95% confidence interval [CI] 0.85-1.00), p-tau/tau ratio (AUC 0.87, P < .001, 95% CI 0.77-0.97), and YKL40 (AUC 0.82, P = .001, 95% CI 0.68-0.97). 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
In a cross-sectional design, pathology was confirmed by autopsy or a pathologically validated CSF total tau-to-β-amyloid ratio (T-tau/Aβ). 4 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using a cross-sectional design, we examined retinal structure in 38 consecutively enrolled patients with FTD and 44 controls using a standard SD-OCT protocol. 4 key findings →
Design: cross-sectional Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Ninety-five individuals from the Wisconsin Registry for Alzheimer's Prevention were included in these cross-sectional analyses. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We analyzed CSF concentrations of neurogranin, β-amyloid (Aβ42), phosphorylated tau (p-tau), and total tau (t-tau) among 132 neurologically normal older adults (mean 64.5, range 55-85), along with bilateral hippocampal volumes and a measure of episodic memory (Auditory Verbal Learning Test, delayed recall). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hyperhomocysteinemia is a risk factor for cognitive decline and dementia, including Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To better understand how sleep/wake dysregulation affects Alzheimer's disease (AD), we compared the cerebrospinal fluid (CSF) orexin and histamine/tele-methylhistamine (HA/t-MHA) levels of 82 patients (41 probable-AD-high level of evidence, 41 mild cognitive impairment MCI-due-to-AD), 24 other neurologic disorders (OND) and 24 controls. 4 key findings →
Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cerebrovascular disease (CVD) and amyloid-β (Aβ) often coexist, but their influence on neurodegeneration and cognition in predementia stages remains unclear. 4 key findings →
Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by interneuronal tau transfer. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
With promising results in recent treatment trials for Alzheimer's disease (AD), it becomes increasingly important to distinguish AD at early stages from other causes for cognitive impairment. 4 key findings →
Participants: 158 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postmortem brain studies of older drivers killed in car accidents indicate that many had Alzheimer disease (AD) neuropathologic changes. 2 key findings →
Participants: 129 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction is the best anatomical correlate of early cognitive impairment in Alzheimer's disease (AD). 4 key findings →
Participants: 210 Evidence: low
Full summary, score breakdown and related studies → Original source
Co-existence of Alzheimer's disease (AD) in normal pressure hydrocephalus (NPH) is a frequent finding, thus a common pathophysiological basis between AD and NPH has been postulated. 2 key findings →
Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source
The 88 patients with AD included 15 with microbleeds only in cortical/subcortical regions (cortical microbleeds) that could be CAA-related, 16 with microbleeds only in deep locations (deep microbleeds), 3 with microbleeds in both cortical and deep locations (mixed microbleeds), and 54 without microbleeds. 4 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
The ratio CSF p-tau/t-tau was significantly higher in the NC group than that in the AD or OD groups (P<0.0005 for each group). 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma tau was negatively correlated with GMD in the medial temporal lobe (MTL), precuneus, thalamus, and striatum. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
When an LP is performed correctly, the procedure is well tolerated and accepted with a low complication rate. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 29,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,037 records (3.5% of the library) are not peer-reviewed — 964 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →